No abstract

The role of physical exercise as a neuroprotective agent against ischemic injury has been extensively discussed. Nevertheless, the mechanisms underlying the effects of physical exercise on cerebral ischemia remain poorly understood. Here, we investigate the hypothesis that physical exercise increases ischemic tolerance by decreasing the induction of cellular apoptosis and glutamate release. Rats (n = 50) were submitted to a swimming exercise protocol for 8 weeks. Hippocampal slices were then submitted to oxygen and glucose deprivation. Cellular viability, pro-apoptotic markers (Caspase 8, Caspase 9, Caspase 3, and apoptosisinducing factor), and glutamate release were analyzed. The percentage of cell death, the amount of glutamate release, and the expression of the apoptotic markers were all decreased in the exercise group when compared to the sedentary group after oxygen and glucose deprivation. Our results suggest that physical exercise protects hippocampal slices from the effects of oxygen and glucose deprivation, probably by a mechanism involving both the decrease of glutamatergic excitotoxicity and apoptosis induction.

ABSTRACT. The co-occurrence of post-stroke behavioral disorders and cognitive impairment has been extensively investigated. However, studies usually do not include social cognition among the assessed cognitive domains. Objective: To investigate the potential association between facial emotion recognition, a measure of social cognition, and behavioral and cognitive symptoms in the subacute phase of ischemic stroke. Methods: Patients admitted to a Stroke Unit with ischemic stroke were followed up to 60 days. At this time point, they were evaluated with the following tools: Mini-Mental State Examination (MMSE); Frontal Assessment Battery (FAB); Visual Memory Test of the Brief Cognitive Battery (VMT); Phonemic Verbal Fluency (F-A-S Test); Digit Span; Facial Emotion Recognition Test (FERT) and Hospital Anxiety and Depression Scale (HADS). A control group composed of 21 healthy individuals also underwent the same evaluation. Results: Eighteen patients with ischemic stroke were enrolled in this study. They had similar age, sex and schooling years compared to controls. Depression symptoms and episodic memory deficits were significantly more frequent in patients compared to controls. The recognition of sadness expression positively correlated with the levels of anxiety and depression, while and the recognition of fear expression negatively correlated with depression in the stroke group. Conclusions: After an ischemic stroke, patients exhibit impairment in social cognition skills, specifically facial emotion recognition, in association with behavioral symptoms.

Obesity represents a serious global public health problem and is characterized by a low-grade chronic inflammatory state, which can increase the risk of comorbidities, such as: atherosclerosis, diabetes and insulin resistance. In this study, we investigated the effects of the genetic deletion of the metabotropic glutamate receptor 5 (mGluR5) on the modulation of obesity features in BACHD mice, a mouse model of Huntington´s disease. For that, we crossed BACHD and mGluR5 knockout mice (mGluR5−/−) in order to obtain the following groups: Wild type (WT), mGluR5−/−, BACHD and BACHD/mGluR5−/− (double mutant mice). Our results showed that the double mutant mice present decreased body weight as compared to BACHD mice at all tested ages and reduced visceral adiposity as compared to BACHD mice at 6 and 12 months of age. Additionally, 12-month-old double mutant mice present increased adipose tissue levels of adiponectin, decreased leptin levels, and increased IL-10/TNF ratio as compared to BACHD mice. Taken together, our data propose that the absence of mGluR5 reduce weight gain and visceral adiposity in BACHD mice, along with a decrease in the inflammatory state in the visceral adipose tissue (VAT), which may indicate that mGluR5 may play a role in adiposity modulation.